After adding exogenous renin, the velocity of angiotensin I generation is faster in plasma of both hypertensive patients and uremic patients than in plasma of normotensive control subjects. This increased reactivity of renin is not due to differences of endogenous substrate activity or concentration. Preliminary evidence suggests that neutral lipids from normal human plasma competitively inhibit renin. The current project objectives are to identify this lipid inhibitor and to determine if a deficiency of this inhibitor accounts for the greater reactivity of renin in hypertensive and uremic plasma.